Effect of Immunization against Angiotensin II on Blood Pressure and on Plasma Aldosterone in the Rabbit

1975 ◽  
Vol 48 (5) ◽  
pp. 413-420
Author(s):  
R. Beckerhoff ◽  
M. Kappeler ◽  
W. Vetter ◽  
H. Armbruster ◽  
W. Siegenthaler

1. Rabbits were actively immunized against angiotensin II (AII). 2. Basal plasma aldosterone concentration was 0.058 ±0.027 pmol/ml (20.7±9.6 pg/ml) (mean±SD) in immunized and 0.056±0.021 pmol/ml (20.2±7.5 pg/ml) in control animals during suppression of adrenocorticotrophic hormone by dexamethasone. When the endogenous formation of AII was stimulated by frusemide, by haemorrhage or by feeding with low sodium diet, a significant increase of plasma aldosterone was observed with no difference between immunized and non-immunized animals. 3. In non-immune rabbits, the average mean arterial blood pressure rose 13 mmHg during the infusion of AII (5 pmol min−1 kg−1) and 27 mmHg during the infusion of 50 pmol min−1 kg−1. In contrast, there was no clear increase in blood pressure in the immunized animals. The blood pressure rose in immune animals (15 mmHg) and in non-immune animals (36 mmHg) during the infusion of 200 pmol min−1 kg−1 AII. Plasma aldosterone rose in all animals in response to each of the three infusions with no significant difference between the two groups. 4. It is concluded that the immunization against AII blocked only the pressor effect of the peptide but had no clear influence on the response of plasma aldosterone to increased AII. Differences between the affinities of the adrenal and vascular AII receptors may explain these findings.

1995 ◽  
Vol 269 (4) ◽  
pp. H1221-H1228
Author(s):  
M. J. Panzenbeck ◽  
C. L. Loughnan ◽  
J. B. Madwed ◽  
R. J. Winquist ◽  
S. E. Fogal

Inhibition of angiotensin-converting enzyme (ACE) inhibits formation of angiotensin II and, by inhibition of kinin metabolism, may also increase vascular bradykinin. The present experiments were done in sodium-depleted, conscious, unrestrained marmosets (n = 5-11) to examine the contribution of bradykinin to ACE inhibitor-induced hypotension. Aortic blood pressure and heart rate (HR) were monitored via telemetry. After sodium depletion (low-sodium diet and furosemide), captopril (1 mg/kg po) caused a significant (P < 0.05) decrease in mean arterial blood pressure (MABP) (-34 +/- 3 mmHg, maximally, from 79 +/- 2 mmHg) but no change in HR compared with vehicle treatment. The bradykinin receptor antagonist HOE-140 (1 mg/kg sc) significantly inhibited the hypotensive response to captopril and caused marked tachycardia (+133 +/- 14 beats/min from 214 +/- 8 beats/min). HOE-140 (1 mg/kg sc) followed by vehicle administration had no effect on MABP but increased HR similarly. The hypotensive response to captopril was inhibited by HOE-140 regardless of the order of administration or the route of captopril administration (by mouth vs. subcutaneously). The hypotensive response to a renin inhibitor, A-72517 (3 mg/kg sc), was not inhibited by prior HOE-140 administration despite a similar HOE-140-induced tachycardia. These data suggest that the hypotensive effect of captopril in sodium-depleted, conscious marmosets is dependent on functional bradykinin B2 receptors. Also, blockade of B2 receptors uncovers marked tachycardia in this model, suggesting a tonic effect of bradykinin on control of HR in marmosets.


1948 ◽  
Vol 5 (6) ◽  
pp. 815-820 ◽  
Author(s):  
Benjamin Rosenberg ◽  
Alfred E. Rosenthal ◽  
Milton B. Rosenbluth

1979 ◽  
Vol 57 (s5) ◽  
pp. 371s-373s ◽  
Author(s):  
Connie S. McCaa ◽  
H.G. Langford ◽  
W. C. Cushman ◽  
R. E. McCaa

1. The response of arterial blood pressure, plasma renin activity and plasma aldosterone concentration to inhibition of angiotensin I converting enzyme (kininase II) with captopril has been studied in patients with severe, treatment-resistant, malignant hypertension. 2. Nine patients with a past history of severe hypertension, supine diastolic blood pressure &gt; 120 mmHg before conventional antihypertensive therapy and resistant to conventional antihypertensive therapy were studied. 3. Captopril administration resulted in a marked decrease in arterial blood pressure and plasma aldosterone concentration and an increase in plasma renin activity. 4. Although arterial blood pressure remained significantly below the values observed during the control period, pressure did tend to increase again after 3 days. Addition of hydrochlorothiazide kept arterial pressure significantly below pretreatment control values.


2021 ◽  
Vol 44 (1) ◽  
pp. 109-120
Author(s):  
Agustina Pungki Astuti ◽  
Didit Damayanti ◽  
Iskari Ngadiarti

The low sodium and Diet Approaches to Stop Hypertension (DASH) are diets for reducing high blood pressure. This study aimed to analyze the effect of nutrition counseling on the DASH diet compared to low sodium diet on blood pressure in hypertensive patients. The study design was an experimental study that randomly allocated 34 respondents to DASH diet and 35 respondents to low sodium diet. The ages of respondents were 43 to 76 years and women were 74.3 percent. Nutrition counseling was conducted by researchers to respondents who visited health center or Posbindu Larangan Utara. Nutritional counseling was conducted for an average of 20 minutes using existing brochures. Low sodium diet emphasizes reducing sodium intake while DASH diet emphasis more on consuming lots of vegetables, fruit, nuts and low-fat products. Variables collected were the characteristics of respondent, disease, drugs taken and nutritional status, while blood pressure using a sphygmomanometer, food intake including sodium were measured before and 2 weeks after nutritional counseling. Results showed that there was a significant difference in diastolic blood pressure after patients were given DASH diet compared to low sodium diet (p 0.05) and there was a significant difference in delta of systolic and diastolic reduction in DASH diet compared to low sodium diet. Test also showed a significant reduction in systolic, diastolic blood pressure and sodium intake (p 0.001) in both diet groups after receiving counseling. It concluded that DASH diet can be recommended to decrease blood pressure in hypertensive patients with consider nutritional status. ABSTRAK  Diet Rendah Garam (RG) dan Diet Approaches to Stop Hypertension (DASH) adalah diet untuk menurunkan tekanan darah tinggi. Penelitian ini bertujuan untuk menganalisa pengaruh konseling gizi diet DASH dibandingkan diet RG terhadap tekanan darah pasien hipertensi. Rancangan penelitian adalah eksperimen yang secara acak mengalokasi diet DASH kepada 34 orang dan diet RG kepada 35 orang responden. Usia responden antara 43 hingga 76 tahun dan sebagian besar perempuan (74,3%). Konseling gizi dilakukan oleh tim peneliti kepada pasien hipertensi yang memeriksakan diri ke puskesmas atau posbindu Larangan Utara. Konseling gizi dilakukan rata-rata 20 menit menggunakan brosur yang sudah ada. Diet RG menekankan pengurangan asupan natrium sedangkan diet DASH lebih menekankan ke banyak konsumsi sayur, buah, kacang-kacangan dan produk rendah lemak. Variabel yang dikumpulkan adalah karakteristik responden, penyakit dan obat yang diminum serta status gizi sedangkan tekanan darah menggunakan sfigmomanometer, asupan makanan, zat gizi termasuk natrium diukur sebelum dan 2 minggu setelah konseling gizi dilakukan. Hasil menunjukkan adanya perbedaan yang bermakna pada tekanan darah diastolik setelah pasien diberi diet DASH dibandingkan dengan pasien yang diberi diet RG (p0,05) dan terdapat perbedaan delta penurunan sistolik dan diastolik bermakna pada diet DASH dibanding diet RG. Analisa juga menunjukkan adanya penurunan tekanan darah sistolik, diastolik dan asupan natrium  yang bermakna (p0.001) pada kedua kelompok diet setelah mendapat konseling diet DASH dan diet RG. Disimpulkan diet DASH dapat direkomendasikan untuk membantu menurunkan tekanan darah pada pasien hipertensi dengan memperhatikan status gizi. Kata kunci: hipertensi, tekanan darah, diet rendah garam, diet DASH


1996 ◽  
Vol 270 (3) ◽  
pp. F406-F410
Author(s):  
K. A. Duggan ◽  
V. Z. Ye ◽  
D. M. Jones ◽  
G. J. Macdonald

Natriuresis in direct response to a gastric sodium stimulus (upper-gut sodium monitor) has paradoxically only been demonstrated in humans and animals on a low-sodium diet preceding each study. It is possible that the low-sodium diet itself induces or suppresses systems that mediate or oppose the ensuing natriuresis. In this study, we sought to determine whether a system activated by this diet, the renin-angiotensin system, mediates the natriuretic response. Specifically, we sought to show whether changes in the circulating concentration of angiotensin II (ANG II) may mediate the renal response to stimulation of the gastric sodium monitor. Male New Zealand White rabbits were randomly assigned to low- (0.008%) or normal (2.2%) sodium diets. After 1 wk on the experimental diet, they received a sodium load intragastrically or intravenously, and plasma ANG II was measured at 0, 5, 10, 30, 60, and 120 min. Urine was collected for 4 h after the sodium load, and plasma sodium was measured at 0, 2, and 4 h. Urinary sodium excretion was greater in the 4 h after gastric than after intravenous sodium administration (P < 0.025) in the rabbits on the low-sodium diet. No significant difference was noted in the rabbits on the normal sodium. In rabbits on the low-sodium diet, there was an immediate and significant decline in plasma ANG II after sodium was administered both intragastrically (P < 0.025) and intravenously (P < 0.05). This decrease was greater after intragastric than intravenous sodium (P < 0.0025), and the difference was still evident at 120 min (P < 0.05). No significant difference in plasma ANG II was found in the normal diet group. We conclude, therefore, that a prolonged decrease in ANG II concentration may play a role in mediating the natriuretic response to the gastric sodium monitor.


1981 ◽  
Vol 61 (s7) ◽  
pp. 441s-444s ◽  
Author(s):  
J. Staessen ◽  
R. Fagard ◽  
P. Lijnen ◽  
L. J. Verschueren ◽  
A. Amery

1. With a double-blind cross-over protocol, 20 hypertensive captopril-treated patients were studied by adding in a variable sequence a placebo and propranolol (80 mg three times a day) to their captopril regimen (200 mg three times a day), during periods each lasting 1 month. During captopril—placebo treatment their diastolic blood pressure remained elevated between 90 and 114 mmHg. 2. The additional administration of propranolol produced a significant hypotensive effect, but no alterations of the plasma angiotensin II and aldosterone concentrations and of the urinary aldosterone excretion occurred. The present data indicate that in captopril-treated patients the hypotensive effect of propranolol is achieved independently of changes in the plasma angiotensin II and aldosterone concentration. 3. The additional administration of propranolol also produced an increase in the serum potassium levels in the absence of any change in the plasma aldosterone concentration or in the urinary aldosterone excretion.


1974 ◽  
Vol 48 (s2) ◽  
pp. 41s-44s
Author(s):  
R. Beckerhoff ◽  
G. Uhlschmid ◽  
W. Vetter ◽  
H. Armbruster ◽  
J. Nussberger ◽  
...  

1. The effect of infusions of equimolar doses of angiotensin II (AII) and of the angiotensin analogue Sar1-Ile8-angiotensin II on arterial blood pressure, plasma aldosterone and plasma renin activity were compared in normal anaesthetized dexamethasone suppressed dogs. 2. Angiotensin II induced a significant increase of blood pressure and of plasma aldosterone whereas plasma renin activity decreased. The blood pressure was only slightly affected by large doses of the analogue. Plasma aldosterone, however, increased and plasma renin activity decreased. These changes were significant but less pronounced than after the infusions of angiotensin II. Plasma aldosterone remained high and renin activity low for 40 min after the infusions of the analogue. 3. The results suggest a strong agonistic potency of Sar1-Ile8-angiotensin II at the adrenal and renal angiotensin receptors, and that it is almost ineffective at the vascular receptors. The inhibition of renin secretion by angiotensin seems not to be related to its vasoconstrictive activity.


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